Adult neurogenesis is functionally associated with AD-like neurodegeneration

Chen, Qian; Nakajima, Akira; Choi, Se Hoon; Xiong, Xiaoli; Sisodia, Sangram S.; Tang, Yaping

doi:10.1016/j.nbd.2007.09.005

Cited by 87 publications

(66 citation statements)

References 55 publications

(75 reference statements)

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“…month-old TgCRND8 compared to non-Tg mice. This increase in BrdU-positive cells may represent an initial compensatory mechanism to enhance cell proliferation in response to A␤PP/A␤ exposure, as proposed by Chen and colleagues [46] and previously observed in TgCNRD8 mice at early stages of the disease [47]. Our results indicate that this initial increase in proliferation does not promote neurogenesis, as no corresponding increase in DCX or BrdU/NeuN-positive cells is observed, possibly because of the toxic environment composed of A␤ [7,8,39].…”

Section: Discussionsupporting

confidence: 78%

“…Other studies report diminished number of newborn neurons reaching maturation [6,7,[42][43][44][45], partly due to impaired survival of newly generated neurons [44]. Chen et al [46] reported increased neurogenesis at early stages of neurodegeneration but not at late stages, suggesting that dynamic changes in neurogenesis were correlated with the severity of neuronal loss in DG, and perhaps serve as compensatory mechanism following neurodegeneration.…”

Section: Discussionmentioning

confidence: 98%

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A Comparative Study Evaluating the Impact of Physical Exercise on Disease Progression in a Mouse Model of Alzheimer’s Disease

Maliszewska-Cyna

Xhima

Aubert

2016

JAD

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Abstract. Evidence suggests that physical exercise can serve as a preventive strategy against Alzheimer's disease (AD). In contrast, much less is known about the impact of exercise when it is introduced after cognitive deficits are established. Using the TgCRND8 mouse model of amyloidosis, we compared the effects of exercise as an intervention strategy aimed at altering disease progression. Voluntary running for 1 month or 2 months was introduced in 3-month-old TgCRND8 mice, which exhibit amyloid-beta (A␤) plaque pathology and cognitive deficits at this age. Specifically, we examined A␤ plaque load, spatial memory, and neurogenesis in the dentate gyrus in the hippocampus. After 1 month of running, TgCRND8 mice spent more time in the novel arm of the Y-maze compared to the familiar arms, indicating improved memory. The levels of doublecortin (a marker of immature neurons) were increased in TgCRND8 mice running for 1 month, but with no significant difference in the number of new mature neurons or plaque burden. As the disease progressed, running prevented further deficits in the Y-maze performance and hippocampal neurogenesis and it reduced plaque load pathology in TgCRND8 mice running for 2 months, compared to non-running transgenics. Therefore, the impact of running on memory, neurogenesis, and amyloid pathology was of greater significance when sustained through later stages of the disease.

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Section: Discussionsupporting

confidence: 78%

Section: Discussionmentioning

confidence: 98%

A Comparative Study Evaluating the Impact of Physical Exercise on Disease Progression in a Mouse Model of Alzheimer’s Disease

Maliszewska-Cyna

Xhima

Aubert

2016

JAD

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“…Interestingly, a similar increase in adult hippocampal cell proliferation (measured by multiple endogenous newborn neuron markers) was found in the subgranular zone of human subjects with AD (88). It has therefore been suggested that this increase may be a compensatory repair mechanism (88,90).…”

Section: Discussionmentioning

confidence: 65%

Cognitive Deficits and Disruption of Neurogenesis in a Mouse Model of Apolipoprotein E4 Domain Interaction

Adeosun

Hou

Zheng

et al. 2014

Journal of Biological Chemistry

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Background: Domain interaction may be the principal pathogenic feature of apoE4 in Alzheimer disease. Results: Young and old mice with mutations causing apoE4 domain interaction showed impaired cognition and a disruption in neurogenesis. Conclusion: Domain interaction mediates apoE4 neuro-pathologies and cognitive phenotype. Significance: Domain interaction is a viable prophylactic target against apoE4 cognitive phenotype and increased susceptibility to Alzheimer disease.

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“…Neurodegenerative and pathological processes promote neurogenesis as described for human Alzheimer's and Huntington's disease patients. 18,19 Previous papers found an increase in the number of neural progenitor cells (NPC) following chronic disease of the spinal cord (either for a long time interval following a spinal trauma or during the course of ALS). 20,21 Nonetheless, none of the studies provide evidence for a net increase in neuron number and the prevalent literature suggests that these NPC tend to differentiate into glial cells.…”

Section: Lithium Astrocytes and Neural Progenitor Cellsmentioning

confidence: 99%

Autophagy and amyotrophic lateral sclerosis: The multiple roles of lithium

Fornai¹,

Longone²,

Ferrucci³

et al. 2008

Autophagy

101

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In a pilot clinical study that we recently published we found that lithium administration slows the progression of Amyotrophic Lateral Sclerosis (ALS) in human patients. This clinical study was published in addition with basic (in vitro) and pre-clinical (in vivo) data demonstrating a defect of autophagy as a final common pathway in the genesis of ALS. In fact, lithium was used as an autophagy inducer. In detailing the protective effects of lithium we found for the first time that this drug stimulates the biogenesis of mitochondria in the central nervous system and, uniquely in the spinal cord, it induces neuronogenesis and neuronal differentiation. In particular, the effects induced by lithium can be summarized as follows: (i) the removal of altered mitochondria and protein aggregates; (ii) the biogenesis of well-structured mitochondria; (iii) the suppression of glial proliferation; (iv) the differentiation of newly formed neurons in the spinal cord towards a specific phenotype. In this addendum we focus on defective autophagy as a "leit motif" in ALS and the old and novel features of lithium which bridge autophagy activation to concomitant effects that may be useful for the treatment of a variety of neurodegenerative disorders. In particular, the biogenesis of mitochondria and the increase of calbindin D 28K-positive neurons, which are likely to support powerful neuroprotection towards autophagy failure, mitochondriopathy and neuronal loss in the spinal cord

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Adult neurogenesis is functionally associated with AD-like neurodegeneration

Cited by 87 publications

References 55 publications

A Comparative Study Evaluating the Impact of Physical Exercise on Disease Progression in a Mouse Model of Alzheimer’s Disease

A Comparative Study Evaluating the Impact of Physical Exercise on Disease Progression in a Mouse Model of Alzheimer’s Disease

Cognitive Deficits and Disruption of Neurogenesis in a Mouse Model of Apolipoprotein E4 Domain Interaction

Autophagy and amyotrophic lateral sclerosis: The multiple roles of lithium

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